Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018133 (graft-versus-host disease)
 18,032 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Homogeneous immunoglobulins are frequently detected in the serum of patients undergoing allogeneic bone marrow transplantation (BMT). The aim of the present study was to further characterize the incidence of this phenomenon and its correlations with laboratory and clinical data. Serum samples were gathered from 29 patients undergoing allogeneic or syngeneic BMT for chronic myeloid leukemia (CML), and serial protein (IgG, IgA and IgM) quantification, electrophoresis and immunofixation were performed. Transient mono- or oligoclonal gammopathies were observed in 23 out of 29 patients between days 20 and 1,750 following transplantation. The presence of homogeneous immunoglobulins was not correlated with the following clinical parameters: graft-versus-host disease, bacterial sepsis, Epstein-Barr virus or cytomegalovirus infection or invasive fungal infection. Therefore, the development of mono- or oligoclonal immunoglobulins may represent a complex disorder of B cell regeneration which may be caused by an intrinsic B cell defect, or a failure in the regenerating T cell system, or both, manifesting itself in a restricted antibody diversity after allogeneic BMT.
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PMID:Homogeneous immunoglobulins following allogeneic bone marrow transplantation. 1271 21

The syndrome of multiple intestinal atresia with immunodeficiency is a rare, invariably fatal congenital disorder. At 16 months of age, a child with this syndrome underwent liver-small bowel transplantation from a 1-of-6 HLA-matched donor. He acquired full enteral tolerance and normal liver function and has never shown evidence of allograft rejection. After mild graft-versus-host disease developed, studies revealed that more than 99% of his CD3(+) lymphocytes and 50% of his CD19(+) lymphocytes were of donor origin, whereas granulocytes and monocytes remained of recipient origin. He synthesizes polyclonal immunoglobulin G (IgG), IgA, and IgM and has developed antibodies to cytomegalovirus (CMV) and parainfluenza 3. His T lymphocytes are predominately CD3(+)CD4(-)CD8(-) with T-cell receptor gammadelta heterodimers and CD3(+)CD4(-)CD8(+) with CD8alphaalpha homodimers, populations consistent with an intraepithelial lymphocyte phenotypic profile. We postulate that he has engrafted a donor intestine-derived immune system and is incapable of rejecting his engrafted organs.
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PMID:Donor immune reconstitution after liver-small bowel transplantation for multiple intestinal atresia with immunodeficiency. 1452 85

Anecdotally, enteroviruses have been reported to cause serious complications post BMT, but the exact impact of these viruses in the post transplant period has not been reported. We prospectively evaluated stool, urine and throat samples for enteroviruses by viral culture together with relevant body fluids by RT-PCR in 64 allograft recipients receiving grafts T-cell depleted by Campath-1H, following both conventional and reduced-intensity conditioning. Seven patients (10.4%) developed nine episodes of enterovirus infections at a median of 146 days post transplant. Four episodes were associated with symptomatic illnesses, which could be attributable to enteroviruses. There was no mortality directly related to enteroviruses. There was no correlation between dose and mode of Campath-1H use, lymphocyte recovery, IgG and IgA levels and enterovirus isolation. Although enteroviruses tended to be more frequent in TBI-based conventional conditioning recipients, the only significant risk factor for enterovirus infection was unrelated donor graft. The low incidence of the severe enterovirus infections could have been related to a low lymphocyte count in this cohort in the absence of GVHD, particularly CD4+ count, which has been implicated in tissue damage in experimental animals. Further studies are needed to define its impact in different allograft settings.
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PMID:Enterovirus infections following T-cell depleted allogeneic transplants in adults. 1468 15

Our understanding of biliary epithelial cells (BEC) in physiobiology and immunology has steadily expanded. BEC transports IgA as well as IgM into bile, synthesizes and secretes various chemokines, cytokines, and expresses adhesion molecules involved in cell interaction and signal transduction. These then suggest a myriad of potential roles for BEC in defense from invading microorganisms as well as the pathogenesis of diverse immunologically driven diseases such as primary biliary cirrhosis (PBC), graft-versus-host disease, and primary sclerosing cholangitis (PSC). Despite the progress, there still remain many areas of BEC biology that require further investigation. Most importantly, it remains to be clarified that the extent to which the immunologic activities observed in BEC represent a BEC response to tissue injury or whether BEC themselves are the active participants in the pathogenesis of various cholestatic immunological diseases, including PBC and PSC.
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PMID:A review of the physiological and immunological functions of biliary epithelial cells: targets for primary biliary cirrhosis, primary sclerosing cholangitis and drug-induced ductopenias. 1555 65

Stem cell transplantation (SCT)-related salivary gland injury and dysfunction result in local and systemic manifestations that may be long lasting and are associated with a high rate of morbidity and increased risk of infection. The salivary antioxidant system may have a major protective role. We, therefore, assessed salivary antioxidant capacity and function in 30 patients who had undergone SCT: 18 males and 12 females whose median age was 36 years (range: 7-58). Salivary gland function was assessed by sialometric and biochemistry means, which included measuring total protein, secretory IgA (SIgA) and the antioxidants peroxidase, uric acid (UA), and total antioxidant status (TAS) in the collected saliva. In patients who developed graft versus host disease (GVHD), we observed a significant decrease of the salivary flow rate, from 0.74 +/- 0.14 ml/minute to 0.19 +/- 0.08 ml/min, pre- and post-SCT, respectively (p < 0.01) with no recovery. In contrast, in patients who underwent autologous or allogeneic SCT and did not develop GVHD, salivary flow rates returned to normal 3-5 months posttransplantation. GVHD also resulted in a concomitant reduction of the salivary protein content and the salivary antioxidant capacity. The TAS levels in the saliva of the GVHD patients were found to be significantly reduced, to about one-third of the base-line value (P < 0.02). The concomitant reduction in salivary flow rate, protein content, and antioxidant capacity may well explain the GVHD-induced oral and gastrointestinal tract (GIT) mucositis, as the saliva constantly swallowed into the GIT losses its usual antioxidant protective roles. In conclusion, our findings may point at a possible new mechanism for the pathogenesis of oral and intestinal mucositis in pre-GVHD patients. Therapy with artificial saliva and free radical scavengers and/or antioxidants (administered either systemically or via oral rinses) thus, may be of clinical relevance.
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PMID:Salivary antioxidant capacity in graft versus host disease. 1680 54

Palifermin (recombinant human keratinocyte growth factor) prevents the development of acute, lethal graft-versus-host disease (GVHD). It does so, at least in part, by protecting cells from injury. Another property of Palifermin is immune regulation. How the latter influences the evolution of GVHD remains uncertain. We explored the effect of Palifermin on GVHD in the DBA/2 --> ((DBA/2)x(C57BL/6))F(1)-hybrid strain combination, a model associated with autoantibody production and glomerulonephritis. Untreated recipients survived until at least day 150 post-induction. Palifermin-treated recipients succumbed between days 50 and 90 with levels of proteinuria of up to 20 g/L, ascites, and rapidly progressive, crescentic glomerulonephritis that was most severe in mice with the greatest levels of proteinuria. Kidney sections from both Palifermin-treated and untreated recipients showed the presence of granular deposits of IgG, IgM, IgA, and C3 in the mesangium and the glomerular basement membrane. Electron microscopy confirmed the extensive glomerular immune complex deposition. Antinuclear and anti-dsDNA antibodies were present in sera from both treated and untreated recipients; however, those in the latter were only detectable if the serum was kept at 37 degrees C, indicating that they were cryoglobulins. IL-4 was detectable only in cultures from Palifermin-treated recipients and the levels of IL-5 and IL-13 were significantly higher in the Palifermin-treated group than in untreated GVHD mice. IFN-gamma was only detectable in untreated GVHD mice. These data suggest that although Palifermin can protect mice with acute GVHD, it exacerbates GVHD in a model associated with autoantibody production and a preponderance of Th2 cytokines.
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PMID:Effect of palifermin in a murine model of graft-versus-host disease (GVHD) associated with Th2 cytokine production, autoantibody production, and glomerulonephritis. 1695 10

Natural killer (NK) cell alloreactions against recipient cells in the setting of bone marrow transplantation have been associated with decreased rates of graft-versus-host disease (GVHD) and improved survival in transplant recipients with myeloid leukemia. These alloreactions are predicted by the absence of recipient HLA class I ligands for donor inhibitory killer Ig-like receptors (KIR). We hypothesized that donor NK cell alloreactions against recipient cells may affect the development of T and B-cell functions and incidence of GVHD in infants with severe combined immunodeficiency (SCID). Of the 156 patients with SCID who had received related bone marrow transplants without pretransplant chemotherapy or posttransplant GVHD prophylaxis, 137 patient-donor pairs were evaluated for the absence of recipient HLA class I ligands for donor inhibitory KIR. Analysis showed that the absence of a KIR ligand had no effect on the incidence or severity of GVHD (RR [corrected] = 0.95, p = 0.84), development of T-cell function (RR [corrected] = 1.05, p = 0.69), production of IgA (p = 0.46) or IgM (p = 0.33), or on 5-year survival (RR [corrected] = 1.21, p = 0.10). Further, in patients possessing native NK cells, the absence of KIR ligands in donors for recipient-inhibitory KIR did not alter transplantation outcomes. This study suggests that inhibitory KIR/HLA interactions do not play a significant role in bone marrow transplantation for SCID.
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PMID:The effect of natural killer cell killer Ig-like receptor alloreactivity on the outcome of bone marrow stem cell transplantation for severe combined immunodeficiency (SCID). 1719 Nov 49

A double-blind, placebo-controlled study was conducted to evaluate the effect of orally administered pilocarpine on unstimulated whole-saliva flow and composition in 28 patients with chronic graft-versus-host disease (cGVHD). Thirteen patients were treated with pilocarpine of 20 mg/day orally for 7 days, and 15 patients with placebo. Unstimulated whole saliva was collected in the morning on four occasions (30 min before pilocarpine or placebo intake, and 1 h, 1 day and 7 days after the first intake). Significantly, higher salivary flow rates, and sodium and total protein outputs were observed in the second samples of pilocarpine-treated patients compared with controls, whereas calcium and IgA outputs were not altered. Changes in these parameters were not significant in the third and fourth samples, although they were higher in the pilocarpine group. Patients who had received pilocarpine expressed satisfaction with their treatment. These data suggest that pilocarpine may improve salivary flow rate and the feeling of xerostomia in patients with cGVHD.
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PMID:Effect of pilocarpine hydrochloride on unstimulated whole saliva flow rate and composition in patients with chronic graft-versus-host disease (cGVHD). 1731 Jan 30

A general review of advances in the treatment of Primary Immunodeficiencies (PID) has been performed. Treatment with immunoglobulins is indicated in cases of humoral immunodeficiencies and in selected cases of combined immunodeficiencies. The use of intramuscular immunoglobulins in the treatment of PID was abandoned after obtaining the intravenous immunoglobulins, since these are much more effective and have fewer adverse effects. Now subcutaneous immunoglobulins are also available. Immunoglobulins help to keep the patients free of symptoms and infections as these substances are able to neutralise infectious agents, modulate and promote the immune response and favour phagocytosis. Adverse effects have been reported in 5-15 % of patients receiving IVIg, and patients with deficiencies of subclasses of IgG with IgA deficiency and/or anti-IgA antibodies are at risk of severe reactions. No severe adverse effects of subcutaneous immuneglobulins have been reported and the medication can be self-administered. The efficacy and safety of IVIg and SCIg are similar and SCIg administered at home is associated with better quality of life. Stem Cell Transplantation (SCT) in Primary Immunodeficiencies is aimed at restoring the number and/or function of lymphocytes or phagocytes. Matched, related or unrelated donors, or related haploidentical donors are selected. HLA class II mismatched unrelated donors are avoided owing to the risk of severe graft versus host disease (GVHD). Stem cells are obtained from bone marrow, cord blood or peripheral blood. Prophylactic immunossupression (as well as donor T lymphocyte depletion in haploidentical and unrelated donors) is performed to avoid or minimize GVHD. Less toxic "reduced intensity" protocols now exist for pre-transplantation conditioning, indicated to avoid graft rejection if there is residual T-lymphocyte immunity in the host. In the majority of Severe Combined Immunodeficiencies (SCID), SCT results in T lymphocytes graft and the antibody immunodeficiency persists in many cases. The results are better the earlier it is performed, with the absence of previous infections, and with the degree of matching. The patient must be maintained in a laminar flow room with broad anti-infectious prophylaxis and with the intravenous administration of gammaglobulin for a variable period. Many other complications can be expected. Gene therapy. Patients with PID are ideal candidates, as they are monogenic, the haematopoietic cells are easily obtained and virus replication is easy within them. Vectors (viruses) "infect" the stem cells of the patient's bone marrow, producing the transfection of the wild (healthy) gene in these cells. Encouraging results have been achieved in X-linked SCID as there are a number of patients who are considered "cured", although neoplastic processes have occurred due to the activation of proto-oncogenes close to the point of insertion of the external gene, using retroviruses as vectors; there are now trials with adenovirus, physical methods (direct injection...) and chemical methods (viral modification, artificial viruses...). Gene therapy has also been performed in patients with Chronic Granulomatous Disease and trials will improve in the future with changes in protocols used in oncology and infectious diseases.
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PMID:Update on the treatment of primary immunodeficiencies. 1792 72

This study was purposed to investigate immune reconstitution at 12 months after allogeneic peripheral blood stem cell transplantation (all-PBSCT) and its relation with the influencing factors such as age, HLA compatibility, graft versus host disease and viral infection. The T lymphocyte subgroups (CD3(+), CD4(+), CD8(+)), B lymphocyte (CD19(+)) and NK (CD16(+)CD56(+)) cells in peripheral blood and serum immunoglobulin concentrations (IgG, IgA and IgM) of 37 patients were analyzed by flow cytometry and scatter turbidimetry, respectively at 1, 3, 6 and 12 months after transplantation. The results showed that CD3(+) cell percentage was (47.5 +/- 23.2)% at 1 month, (75.1 +/- 6.4)% at 3 months, (69.7 +/- 12)% at 6 months and (71.7 +/- 4.2)% at 12 months. CD4(+) cell percentage was (13.3 +/- 6.4)% at 1 month, (20.2 +/- 11.4)% at 3 months, (46.9 +/- 10.3)% at 6 months and (29.1 +/- 18.7)% at 12 months. CD8(+) cell percentage was (43.1 +/- 23.2)% at 1 month, (42.6 +/- 16.9)% at 3 months, (69.7 +/- 12)% at 6 months and (47 +/- 5.6)% at 12 months. CD16(+)56(+) cell percentage was (14.4 +/- 8.4)% at 1 month, (15.9 +/- 7.6)% at 3 months, (14.7 +/- 6.6)% at 6 months and (13.6 +/- 3.4)% at 12 months. CD19(+) cell percentage was (6.4 +/- 5.6)% at 1 month, (11.7 +/- 2.4)% at 3 months, (13.3 +/- 7.3)% at 6 months and (16.7 +/- 5.7)% at 12 months. The serum concentration of IgA was (0.37 +/- 0.14) g/L at 1 month, (0.28 +/- 0.21) g/L at 3 months, (0.42 +/- 0.18) g/L at 6 months and (0.53 +/- 0.34) g/L at 12 months. The serum concentration of IgG was (12.7 +/- 3.8) g/L at 1 month, (16.3 +/- 5.2) g/L at 3 months, (14.3 +/- 6.2) g/L at 6 months and (15.4 +/- 6.9) g/L at 12 months. The serum concentration of IgM was (0.56 +/- 0.24) g/L at 1 month, (0.64 +/- 0.16) g/L at 3 months, (1.1 +/- 0.35) g/L at 6 months and (1.2 +/- 0.28) g/L at 12 months. There were no significant differences between percentage of T lymphocyte subgroups in peripheral blood and serum immunoglobulin concentrations of the patients > or = 45 years old and the patients < 45 years old. The CD19(+) cell percentage of the patients with chronic GVHD at 12 month was less than that of the other ones at 12 months after transplantation. CD4(+) and CD19(+) cell percentage recovery in the patients of haploidentical transplantation was later than that in patients of HLA complete identical transplantation. The CD4(+)/CD8(+) cell ratio and CD4(+) cell percentage of those patients infected with herpes zoster were significantly lower than those without herpes zoster. It is concluded that the CD3(+) cell percentage begins to recover at 3 months after allo-PBSCT. CD4(+) cell percentage begins to recover at 6 months after allo-PBSCT. CD8(+) cell percentage begins to recover at 1 month after allo-PBSCT. B cell percentage recovers at 3 to 6 months after allo-PBSCT. NK cell percentage recovers at 1 to 3 months after allo-PBSCT. The serum concentration of IgG recovers to normal at 1 month after transplantation which is associated with routine infusion of immunoglobulin. The concentration of IgM gradually recovers to normal at 3 months after transplantation. The concentration of IgA does not recover to normal at 12 months after transplantation. The function of B cells recovers slowly in patients with cGVHD. The CD4(+) cell absolute value and CD4(+)/CD8(+) ratio significantly decrease in patients with herpes zoster.
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PMID:[Immune reconstitution after allogeneic peripheral blood stem cell transplantation]. 1892 11


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